The impact of bowl size, program setup, and blood hematocrit on the performance of a discontinuous autotransfusion system.

BACKGROUND: Cell salvage is an essential element in the concept of blood management. Modern devices provide different bowl sizes and sensor-directed programs to optimally adjust to varying clinical situations. STUDY DESIGN AND METHODS: In an experimental performance study, the discontinuous autotransfusion device XTRA (LivaNova/Sorin) was evaluated using fresh donor blood anticoagulated with heparin 5 U/mL and adjusted to a hematocrit of 10% or 25%, representing orthopedic or cardiac surgery. Test blood was processed with the autotransfusion device XTRA in four different bowls (55 mL, 125 mL, 175 mL, and 225 mL) and in three different program modes (a standard program, an optimized program, and an emergency program). RESULTS: Processing speed increased with bowl size and with the emergency program (range, 6.4-29.8 mL red blood cells [RBCs]/min). The RBC recovery rate exceeded 90% for all bowls and programs except the 55-mL bowl with the emergency program. Plasma elimination exceeded 95% for all bowls and programs except the 225-mL bowl with the emergency and standard programs. Maximal RBC recovery (range, 94.7%-97.6%) and plasma elimination (range, 98.7%-99.5%) were obtained with the medium-sized bowls (125 mL and 175 mL) and the optimized program. Elimination rates for potassium or plasma free hemoglobin were consistently lower than for protein or albumin and were highest for heparin. CONCLUSIONS: Increased hematocrit and RBC recovery rates are obtained with the optimized program Popt with the discontinuous autotransfusion device. The emergency program Pem speeds up the process but leads to RBC loss and reduced plasma elimination rates; therefore, it should be restricted to emergency situations. All four different sized bowls have high performance. Plasma elimination is represented best by protein or albumin elimination rates.

Adenosine A2A and A2B Receptor Substantially Attenuate Ischemia/Reperfusion Injury in Septic rat Hearts.

INTRODUCTION: Mechanical and morphological ischemia and reperfusion (I/R) injury is reduced in septic hearts. The mechanism behind this "cardioprotection" is less well understood. As adenosine receptors play a major role for cardioprotection in non-septic hearts, we investigated the influence of adenosine receptors in a model of I/R in septic hearts. METHODS: SHAM operation or cecal ligation and puncture (CLP) was performed in adult male Wistar rats (n = 60). After 24 h of incubation, hearts were isolated and randomly assigned to a group with or without adenosine receptor (Ador) antagonists (SCH 58261 and MRS 1706) administered before reperfusion. Ischemia and reperfusion lasted for 40 min each. Cardiac function of the heart was determined by measuring left ventricular pressure (LVP). RESULTS: Before I/R, CLP hearts showed a significant mechanical left ventricular impairment (CLP: 63 ± 5 mmHg vs. SHAM: 104 ± 6 mmHg. After I/R, left ventricular function was significantly reduced in SHAM (24 ± 32 mmHg), but not in CLP hearts (65 ± 13 mmHg). mRNA expression for the AdorA2a and AdorA2b was significantly increased in CLP, but not in SHAM hearts. LVP of CLP hearts deteriorated when AdorA2a and AdorA2b were blocked. CONCLUSIONS: The morphological and functional I/R injury in septic animals is less pronounced compared to non-septic animals. By a combined blockade of AdorA2a and AdorA2b this "cardioprotective" effect is nearly abolished in septic hearts. This is the first study showing, that AdorA2a and AdorA2b may play an important role for a reduced functional I/R injury in the septic heart.

The impact of crystalloidal and colloidal infusion preparations on coronary vascular integrity, interstitial oedema and cardiac performance in isolated hearts.

INTRODUCTION: Recent data suggested an interaction between plasma constituents and the endothelial glycocalyx to be relevant for vascular barrier function. This might be negatively influenced by infusion solutions, depending on ionic composition, pH and binding properties. The present study evaluated such an influence of current artificial preparations. METHODS: Isolated guinea pig hearts were prepared in a modified Langendorff mode and perfused with Krebs-Henseleit buffer augmented with 1g% human albumin. After equilibration the perfusion was switched to replacement of one half buffer by either isotonic saline (NaCl), ringer's acetate (Ri-Ac), 6% and 10% hydroxyethyl starch (6% and 10% HES, resp.), or 4% gelatine (Gel), the artificial colloids having been prepared in balanced solution. We analysed glycocalyx shedding, functional integrity of the vascular barrier and heart performance. RESULTS: While glycocalyx shedding was not observed, diluting albumin concentration towards 0.5g% by artificial solutions was associated with a marked functional breakdown of vascular barrier competence. This effect was biggest with isotonic saline and significantly attenuated with artificial colloids, the difference in the pressure dependent transvascular fluid filtration (basal vs. during infusion in groups NaCl, Ri-Ac, 6% HES, 10% HES and Gel, n = 6 each) being 0.31 ± 0.03 vs. 1.00 ± 0.04; 0.27 ± 0.03 vs. 0.81 ± 0.03; 0.29 ± 0.03 vs. 0.68 ± 0.02; 0.32 ± 0.03 vs. 0.59 ± 0.08 and 0.31 ± 0.04 vs. 0.61 ± 0.03 g/5min, respectively. Heart performance was directly related to pH value (7.38 ± 0.06, 7.33 ± 0.03, 7.14 ± 0.04, 7.08 ± 0.04, 7.25 ± 0.03), the change in the rate pressure product being 21,702 ± 1969 vs. 21,291 ± 2,552; 22,098 ± 2,115 vs. 14,114 ± 3,386; 20,897 ± 2,083 vs. 10,671 ± 1,948; 21,822 ± 2,470 vs. 10,047 ± 2,320 and 20,955 ± 2,296 vs. 15,951 ± 2,755 mmHg × bpm, respectively. CONCLUSIONS: It appears important to maintain the pH value within a physiological range to maintain optimal myocardial contractility. Using colloids prepared in calcium-containing, balanced solutions for volume replacement therapy may attenuate the breakdown of vascular barrier competence in the critically ill.

Modulation of immune functions in polymorphonuclear neutrophils induced by physostigmine, but not neostigmine, independent of cholinergic neurons.

BACKGROUND: Cholinesterase inhibitors (Ch-I) improve survival in experimental sepsis consistent with activation of the cholinergic-anti-inflammatory-pathway. So far, less is known about whether Ch-I have a direct immunomodulatory effect on immune cells (polymorphonuclear neutrophils, PMN) in the absence of cholinergic neurons. We investigated the concentration-response-effects of physostigmine and neostigmine on the oxidative burst activity (human and rat PMN) and the expression of adhesion molecules on the surface of human PMN under in vitro conditions. METHODS: PMN from 10 healthy humans or 10 rats were pretreated with 2, 10, 24, 97 µM physostigmine or 3, 15, 30, 150 µM neostigmine, primed with tumor-necrosis-factor-alpha (TNF-alpha) followed by stimulation with n-formyl-methionyl-leucylphenylalanine (fMLP) or stimulated with phorbol-12-myristate-13-acetate (PMA). Human and rat samples were assessed by flow cytometry for the generation of oxidative free radicals. Stimulated human PMN were additionally incubated with antibodies against Mac-1 (CD11b) or L-selectin (CD62l). RESULTS: Physostigmine and neostigmine did not alter oxidative burst activity or the expression of adhesion molecules of PMN induced by receptor-dependent activators like fMLP or TNF-alpha/fMLP (rat and human PMN, p=n.s.). Physostigmine, but not neostigmine, inhibited the protein-kinase-C-mediated oxidative burst activity by PMA in a dose-dependent manner (rat and human PMN, p<0.05). Physostigmine, in the concentration range tested, suppressed the expression of CD11b following stimulation with PMA not significantly (human PMN: control: 63.1±10.7 vs. 97 µM physostigmine: 49.9±12.8 MESF, p=n.s.). CONCLUSION: While neostigmine has no effect on functional and phenotypic changes of PMN, the lipid soluble Ch-I physostigmine causes a dose dependent reduction in PMA-induced oxidative burst, independent of neuronal released acetylcholine.

Cardiac effects of induction agents in the septic rat heart.

INTRODUCTION: The current debate about the side effects of induction agents, e.g. possible adrenal suppression through etomidate, emphasizes the relevance of choosing the correct induction agent in septic patients. However, cardiovascular depression is still the most prominent adverse effect of these agents, and might be especially hazardous in septic patients presenting with a biventricular cardiac dysfunction--or so-called septic cardiomyopathy. Therefore, we tested the dose-response direct cardiac effects of clinically available induction agents in an isolated septic rat heart model. METHODS: A polymicrobial sepsis was induced via cecal ligation and single puncture. Hearts (n = 50) were isolated and randomly assigned to five groups, each receiving etomidate, s(+)-ketamine, midazolam, propofol, or methohexitone at concentrations of 1 x 10-8 to 1 x 10-4 M. Left ventricular pressure, contractility and lusitropy, and coronary flow were measured. Cardiac work, myocardial oxygen delivery, oxygen consumption, and percentage of oxygen extraction were calculated. RESULTS: All of the induction agents tested showed a dose-dependent depression of cardiac work. Maximal cardiac work dysfunction occurred in the rank order of s(+)-ketamine (-6%)